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A brain-enriched circular RNA controls excitatory neurotransmission and restricts sensitivity to aversive stimuli

ABSTRACT: A brain-enriched circular RNA controls excitatory neurotransmission and restricts sensitivity to aversive stimuli

PROVIDER: PRJNA1032476 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26535200.fastq.gz	Fastqsanger.gz
	SRR26535201.fastq.gz	Fastqsanger.gz
	SRR26535202.fastq.gz	Fastqsanger.gz
	SRR26535203.fastq.gz	Fastqsanger.gz
	SRR26535204.fastq.gz	Fastqsanger.gz

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A brain-enriched circular RNA controls excitatory neurotransmission and restricts sensitivity to aversive stimuli

Project description:Circular RNAs are a large class of non-coding RNAs present in all eukaryotic taxa. Despite the identification of thousands of circular transcripts, the biological significance of most of them remains largely unexplored, partly due to the lack of effective methods for generating loss-of-function animal models. In this study, we focused on circTulp4, a highly abundant circRNA that is enriched in the brain and synaptic compartments. By creating a circTulp4-deficient mouse model, in which we mutated the splice acceptor site responsible for generating circTulp4 without affecting the corresponding linear mRNA or protein levels, we were able to conduct a comprehensive phenotypic analysis. Our results demonstrate that circTulp4 is critical in regulating neuronal and brain physiology, modulating the strength of excitatory neurotransmission and sensitivity to aversive stimuli. This study provides compelling evidence that circRNAs can regulate biologically relevant functions in neurons, with modulatory effects at multiple levels of the phenotype, establishing a proof-of-principle for the regulatory role of circRNAs in neural processes.

2024-04-13 | GSE246304 | GEO

A brain-enriched circular RNA controls excitatory neurotransmission and restricts sensitivity to aversive stimuli

Project description:The biological significance of circular RNAs remains largely unexplored due to the lack of loss-of-function animal models. In this study, we focused on circTulp4, a highly abundant circRNA that is enriched in the brain and synaptic compartments. We created a circTulp4-deficient (CD) mouse model and conducted a comprehensive phenotypic analysis. To test whether the electrophysiological phenotype observed in CD mice was explained by an alteration in the levels of synaptic proteins, we prepared pure synaptosomal fractions and conducted a quantitative proteomic analysis. Label-free quantification of CD and wildtype synaptic proteomes was performed by using an ion mobility-enhanced data-independent acquisition (DIA) workflow with alternating low and elevated energy (referred to as UDMSE). We quantified >1800 proteins and concluded that the protein composition of the synaptosomal compartment is preserved in CD mice.

2024-04-15 | PXD045787 | Pride

Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools

Project description:Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools

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Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools

Project description:Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools

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Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools

Project description:The ketogenic diet (KD) is a common dietary intervention for treating seizures in intractable childhood epilepsies and has been proposed to improve disease outcome in neurodegenerative disorders. Despite its clinical applications, we know little about how this diet impacts brain circuitry and neuronal function to elicit its protective effects. Here, we examined the impact of the KD on hippocampal function through integrative analysis of gene expression, epigenetics and neurotransmission. We found that KD induces profound transcriptional reprogramming of the hippocampus, including altered expression of numerous synaptic genes. Proteomic analysis of histone variants and post-translational modifications also revealed significant changes in activating and repressive epigenetic marks in the hippocampus of KD mice. To determine how transcriptional and epigenetic rewiring of the hippocampus under KD impacts neurotransmission, we performed electrophysiological recordings to examine synaptic dynamics and synaptic summation at CA3-CA1 synapses. We found that KD diminishes synaptic gain and dampens short-term plasticity at excitatory synapses, resulting in reduced summation of synaptic inputs at the circuit level. We determined that the dampening of synaptic gain was due to a reduction in size of the readily releasable as well as the total of synaptic vesicles in excitatory but not inhibitory synapses. Our findings show that the ketogenic diet triggers synaptic remodeling in the hippocampus, driven by broad transcriptional and epigenetic changes that reduce synaptic vesicle pools and short-term plasticity at excitatory synapses ultimately dampening excitatory synaptic gain and integration at the circuit level. These synaptic adaptations may represent a major mechanism underlying the anti-epileptic effects of this diet.

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Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools

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RIPK3 promotes neuronal survival by suppressing excitatory neurotransmission during CNS viral infection

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Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools

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